IL-23 induces receptor activator of NF-kappa B ligand expression on CD4(+) T cells and promotes osteoclastogenesis in an autoimmune arthritis model
SCIE
SCOPUS
- Title
- IL-23 induces receptor activator of NF-kappa B ligand expression on CD4(+) T cells and promotes osteoclastogenesis in an autoimmune arthritis model
- Authors
- Ju, JH; Cho, ML; Moon, YM; Oh, HJ; Park, JS; Jhun, JY; Min, SY; Cho, YG; Park, KS; Yoon, CH; Min, JK; Park, SH; Sung, YC; Kim, HY
- Date Issued
- 2008-07-15
- Publisher
- AMER ASSOC IMMUNOLOGISTS
- Abstract
- IL-23, a clinically novel cytokine, targets CD4(+) T cells. Recent IL-1Ra(-/-) mouse studies have demonstrated that IL-23 indirectly stimulates the differentiation of osteoclast precursors by enhancing IL-17 release from CD4(+) T cells. IL-17, in turn, stimulates osteoclastogenesis in osteoclast precursor cells. In this study, we found that IL-23 up-regulates receptor activator of NF-kappa B ligand expression by CD4(+) T cells, and thus contributes to osteoclastogenesis. This indirect pathway is mediated by NF-kappa B and STAT3. We have also demonstrated that IL-23 can influence osteoclastogenesis positively under the special conditions in the IL-1-dominant milieu of IL-1Ra(-/-) mice. We propose that IL-23-enhanced osteoclastogenesis is mediated mainly by CD4(+) T cells. The results of this study show that IL-23 is a promising therapeutic target for the treatment of arthritis-associated bone destruction.
- Keywords
- TUMOR-NECROSIS-FACTOR; RHEUMATOID-ARTHRITIS; BONE DESTRUCTION; FACTOR-ALPHA; RANKL; EROSION; INTERLEUKIN-17; STIMULATION; INVOLVEMENT; INDUCTION
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/22616
- DOI
- 10.4049/jimmunol.181.2.1507
- ISSN
- 0022-1767
- Article Type
- Article
- Citation
- JOURNAL OF IMMUNOLOGY, vol. 181, no. 2, page. 1507 - 1518, 2008-07-15
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